Autophagy and Hallmarks of Cancer
Autophagy is a catabolic program that is responsible for the degradation of dysfunctional or unnecessary proteins and organelles to maintain cellular homeostasis. Mechanistically, it involves the formation of double-membrane autophagosomes that sequester cytoplasmic material and deliver it to lysoso...
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Published in | Critical reviews in oncogenesis Vol. 23; no. 5-6; p. 247 |
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Main Authors | , , , , , , , , |
Format | Journal Article |
Language | English |
Published |
United States
2018
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Subjects | |
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Abstract | Autophagy is a catabolic program that is responsible for the degradation of dysfunctional or unnecessary proteins and organelles to maintain cellular homeostasis. Mechanistically, it involves the formation of double-membrane autophagosomes that sequester cytoplasmic material and deliver it to lysosomes for degradation. Eventually, the material is recycled back to the cytoplasm. Abnormalities of autophagy often lead to human diseases, such as neurodegeneration and cancer. In the case of cancer, increasing evidence has revealed the paradoxical roles of autophagy in both tumor inhibition and tumor promotion. Here, we summarize the context-dependent role of autophagy and its complicated molecular mechanisms in the hallmarks of cancer. Moreover, we discuss how therapeutics targeting autophagy can counter malignant transformation and tumor progression. Overall, the findings of studies discussed here shed new light on exploiting the complicated mechanisms of the autophagic machinery and relevant small-molecule modulators as potential antitumor agents to improve therapeutic outcomes. |
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AbstractList | Autophagy is a catabolic program that is responsible for the degradation of dysfunctional or unnecessary proteins and organelles to maintain cellular homeostasis. Mechanistically, it involves the formation of double-membrane autophagosomes that sequester cytoplasmic material and deliver it to lysosomes for degradation. Eventually, the material is recycled back to the cytoplasm. Abnormalities of autophagy often lead to human diseases, such as neurodegeneration and cancer. In the case of cancer, increasing evidence has revealed the paradoxical roles of autophagy in both tumor inhibition and tumor promotion. Here, we summarize the context-dependent role of autophagy and its complicated molecular mechanisms in the hallmarks of cancer. Moreover, we discuss how therapeutics targeting autophagy can counter malignant transformation and tumor progression. Overall, the findings of studies discussed here shed new light on exploiting the complicated mechanisms of the autophagic machinery and relevant small-molecule modulators as potential antitumor agents to improve therapeutic outcomes. |
Author | Sastry, Namratha Alvarez, Angel A Wan, Xuechao Feng, Haizhong Cheng, Shi-Yuan Huang, Tianzhi Song, Xiao Hu, Bo Yang, Yongyong |
Author_xml | – sequence: 1 givenname: Tianzhi surname: Huang fullname: Huang, Tianzhi organization: Ken & Ruth Davee Department of Neurology, Lou & Jean Malnati Brain Tumor Institute, Robert H. Lurie Comprehensive Cancer Center, Northwestern University Feinberg School of Medicine, Chicago, IL – sequence: 2 givenname: Xiao surname: Song fullname: Song, Xiao organization: Ken & Ruth Davee Department of Neurology, Lou & Jean Malnati Brain Tumor Institute, Robert H. Lurie Comprehensive Cancer Center, Northwestern University Feinberg School of Medicine, Chicago, IL – sequence: 3 givenname: Yongyong surname: Yang fullname: Yang, Yongyong organization: Ken & Ruth Davee Department of Neurology, Lou & Jean Malnati Brain Tumor Institute, Robert H. Lurie Comprehensive Cancer Center, Northwestern University Feinberg School of Medicine, Chicago, IL – sequence: 4 givenname: Xuechao surname: Wan fullname: Wan, Xuechao organization: Ken & Ruth Davee Department of Neurology, Lou & Jean Malnati Brain Tumor Institute, Robert H. Lurie Comprehensive Cancer Center, Northwestern University Feinberg School of Medicine, Chicago, IL – sequence: 5 givenname: Angel A surname: Alvarez fullname: Alvarez, Angel A organization: Ken & Ruth Davee Department of Neurology, Lou & Jean Malnati Brain Tumor Institute, Robert H. Lurie Comprehensive Cancer Center, Northwestern University Feinberg School of Medicine, Chicago, IL – sequence: 6 givenname: Namratha surname: Sastry fullname: Sastry, Namratha organization: Ken & Ruth Davee Department of Neurology, Lou & Jean Malnati Brain Tumor Institute, Robert H. Lurie Comprehensive Cancer Center, Northwestern University Feinberg School of Medicine, Chicago, IL – sequence: 7 givenname: Haizhong surname: Feng fullname: Feng, Haizhong organization: State Key Laboratory of Oncogenes and Related Genes, Renji-Med X Clinical Stem Cell Research Center, Ren Ji Hospital, School of Medicine, Shanghai Jiao Tong University, Shanghai, China – sequence: 8 givenname: Bo surname: Hu fullname: Hu, Bo organization: Ken & Ruth Davee Department of Neurology, Lou & Jean Malnati Brain Tumor Institute, Robert H. Lurie Comprehensive Cancer Center, Northwestern University Feinberg School of Medicine, Chicago, IL – sequence: 9 givenname: Shi-Yuan surname: Cheng fullname: Cheng, Shi-Yuan organization: Ken & Ruth Davee Department of Neurology, Lou & Jean Malnati Brain Tumor Institute, Robert H. Lurie Comprehensive Cancer Center, Northwestern University Feinberg School of Medicine, Chicago, IL |
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SubjectTerms | Animals Autophagosomes Autophagy - drug effects Autophagy - genetics Biomarkers Cell Transformation, Neoplastic - genetics Cell Transformation, Neoplastic - metabolism Drug Resistance, Neoplasm Energy Metabolism Epigenesis, Genetic Humans Molecular Targeted Therapy Neoplasm Invasiveness Neoplasm Metastasis Neoplasms - diagnosis Neoplasms - etiology Neoplasms - metabolism Neoplasms - therapy RNA Processing, Post-Transcriptional Transcription, Genetic |
Title | Autophagy and Hallmarks of Cancer |
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